Although intrauterine growth retardation complicates 4-5% of all pregnancies, and the fetus is particularly susceptible to acute stress, very little is known about the physiologic mechanisms involved in the fetus' inability to tolerate stress, or how the mechanisms might be modified. The broad objective of these studies is to investigate the response of the fetus, which is growth retarded due to uteroplacental insufficiency, to acute stress, and to determine if these responses may be modified. Fetal growth retardation is produced by a gradual embolization of the uteroplacental vascular bed with non-radioactive microspheres. The development of autonomic regulation is studied. The effects of acute hypoxemia, or combined hypoxemia and acidemia on the cardiovascular and metabolic responses is investigated. Beta-adrenergic agents will be used to determine if the responses may be modified in a beneficial manner. BIBLIOGRAPHIC REFERENCES: Pickart, L.R., Creasy, R.K. and Thaler, M.M.: Polycythemia and Hyperfibrinogenemia as Factors in Experimental Intrauterine Growth Retardation. Am. J. Obstet. Gynec., 124(3):268-271, 1976. Char, U.C. and Creasy, R.K.: Glucose and Oxygen Metabolism in Normally Oxygenated and Spontaneously Hypoxemic Fetal Lambs. Am. J. Obstet. Gynec., 127(5): 499-504, 1977.